Chemicals that block a signal that prevents damaged nerve cells re-growing
have been identified by US scientists.

The compounds stimulated the regeneration of isolated damaged rat neurons
in the laboratory - and the researchers hope they might be used to help
treat spinal cord injury and contribute to a better understanding of multiple
sclerosis in people.

Neurons are sheathed in myelin - a fatty substance that insulates electrical
signals passing along the axon. But when a neuron is damaged, myelin sends
chemical signals that prevent it regenerating.

One of the three previously identified signalling pathways involves
an interaction between myelin-associated glycoprotein (MAG), on the inner
surface of the myelin sheath, and lipids called gangliosides on the outer
surface of the axons.

A team led by Ronald Schnaar at Johns Hopkins University in Baltimore
has now pinpointed four ways of blocking this pathway. These include using
an antibody to prevent gangliosides bonding with MAG, and an enzyme called
neuroaminidase, which prevents the interaction by destroying a critical
part of the gangliosides.

"Profoundly complex"

Other teams have succeeded in over-riding the two other known myelin
pathways that block axon re-growth. But each single method triggers only
limited regeneration. Schnaar hopes that a combined treatment might be
more effective. Ben Barres, a neurobiologist at Stanford University, California,
agrees: "All of these three steps are very important."

Schnaar cautions that spinal cord injuries are "profoundly complex.
It's still unclear what's going to be required to get functional recovery
in human nerve injuries," he says.

But he hopes his research could also contribute to new treatments for
multiple sclerosis. The disease involves a progressive loss of myelin around
neurons. But researchers think degeneration of the axons themselves, as
well as myelin degradation, could also contribute to the symptoms.

Schnaar presented his research at a meeting of the American Chemical
Society in Orlando, Florida.